It is known that elderly individuals show susceptibility to influenza A virus. One reason for this susceptibility is a reduced ability of elderly immune system to produce type I IFNs in response to influenza A virus.

In contrast, aging mice do not show such susceptibility to influenza A virus. Mouse does not express Mx1, a dynamin-like guanosine triphosphatase that blocks primary transcription of influenza in humans. To make mouse model "usable" for studying human response influenza A virus, the authors created Mx1+ mice. Mx1+ mice were resistant to experimental influenza A virus infection and this resistance was dependent on Tlr7 and Mavs(both molecules are involved in anti-viral response).

Interestingly, while Mx1+ mice double deficient for Tlr7–/– × Mavs–/– were susceptible to influenza A virus infection, Mx1+ mice triple deficient for Tlr7–/– × Mavs–/–× Casp1/11–/– were resistant to influenza A virus infection even though both showed similar viral burden (Of note, Tlr7–/– × Mavs–/–× Casp1/11–/– mice were eventually cleared the virus by 30 days after infection).

Moreover, Mx1+ mice triple deficient for Tlr7–/– × Mavs–/–× Casp1/11–/– were resistant to influenza A virus infection even though they too showed similar secondary bacterial "bloom" in their airways.